Global Resistance of Neisseria gonorrhoeae

When Theory Becomes Reality

David A. Lewis


Curr Opin Infect Dis. 2014;27(1):62-67. 

In This Article

Gonococcal Resistance to Penicillins and Tetracyclines

Following the early demise of sulphonamides and the contemporary introduction of penicillin in the early 1940s, penicillin became established as the mainstay of therapy for gonorrhoea.[3] Increasing curative doses were required to combat the rise in penicillin minimum inhibitory concentrations (MICs) that were observed from the 1950s onwards. Chromosomally mediated penicillin resistance, due to a combination of mutations in several genes (e.g. penA, penB, mtrR and its promoter), was reported in many parts of the world during the 1960s.[3] In the mid-1970s, plasmid-mediated penicillinase-producing N. gonorrhoeae (PPNG) strains emerged. By the late 1970s, penicillin was no longer effective as a treatment for gonorrhoea in many regions of the world.

Decreased susceptibility to tetracycline, and eventual emergence of chromosomal resistance due to multiple genetic mutations (e.g. rpsJ, penB, mtrR and its promoter), followed a similar course to penicillin. In the 1980s, gonococci were detected with high-level tetracycline resistance due to plasmid-mediated expression of the TetM determinant. Tetracycline-resistant N. gonorrhoeae strains rapidly spread globally, and the TetM-encoding plasmid was frequently found in PPNG strains.